The in vitro effect of protein synthesis inhibitors on FcIgG receptor (FcR) expression was studied in secondary cultures of fetal rat brain cells (FBC). Hemadsorption of antibody-coated sheep erythrocytes was used for the detection of FcR-positive cells. The addition of actinomycin D 0.5 and 2.5 micrograms/ml or cycloheximide 1.0 and 5.0 micrograms/ml to the growth medium did not change the FcR activity after 4 and 12 h. When the cells were cultured in medium containing hydrocortisone 10(-6) and 10(-7) M for 1, 2 or 3 days, the number of FcR-positive cells increased markedly. Confluent cultures of FBC and FBC undergoing in vitro neoplastic transformation were FcR negative. Hydrocortisone did not induce FcR activity in these cultures. The results indicate that the persistence of FcR on cultured FBC is not dependent on de novo protein synthesis. Hydrocortisone seems to prolong the period of FcR expression in FcR-positive cells.